ArticleJournal of virology2013
Upregulation of CHOP/GADD153 during coronavirus infectious bronchitis virus infection modulates apoptosis by restricting activation of the extracellular signal-regulated kinase pathway.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 147 citations in OpenAlex.
- Coronavirus M protein disperses the trans-Golgi network and inhibits anterograde protein trafficking in the secretory pathway.PLoS pathogens · 2026Article
- Chemical modulation of the unfolded protein response reveals an antiviral role for the PERK pathway in human coronavirus 229E infection.RSC chemical biology · 2026Article
- Infectious Bronchitis Virus Activates the Aryl Hydrocarbon Receptor During In Vitro Infection.Veterinary sciences · 2025Article
- Multi-Faceted Roles of Stress Granules in Viral Infection.Microorganisms · 2025Review
- Exploring melatonin's signalling pathways in the protection against age-related skin deterioration.Pharmacological reports : PR · 2025Review
- Human coronaviruses: activation and antagonism of innate immune responses.Microbiology and molecular biology reviews : MMBR · 2025Review
- Modulation of viral replication, autophagy and apoptosis by induction and mutual regulation of transcription factors EB and E3 during coronavirus infection.Frontiers in microbiology · 2025Article
- Role of endoplasmic reticulum stress in cell apoptosis induced by duck hepatitis A virus type 1 infection.Frontiers in immunology · 2025Article
- Systems pharmacology-based optimization of Ma Xing Shi Gan components for the enhanced treatment of chick health issues caused by infectious bronchitis virus.Frontiers in cellular and infection microbiology · 2025Article
- COVID-19 related neurological manifestations in Parkinson's disease: has ferroptosis been a suspect?Cell death discovery · 2024Review
- ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor.Biology · 2024Review
- Human Betacoronavirus OC43 Interferes with the Integrated Stress Response Pathway in Infected Cells.Viruses · 2024Article
- Duck Tembusu virus NS3 protein induces apoptosis by activating the PERK/PKR pathway and mitochondrial pathway.Journal of virology · 2023Article
- Porcine Epidemic Diarrhea Virus and Its nsp14 Suppress ER Stress Induced GRP78.International journal of molecular sciences · 2023Article
- Article
- Auto-immunoproteomics analysis of COVID-19 ICU patients revealed increased levels of autoantibodies related to the male reproductive system.Frontiers in physiology · 2023Article
- DDIT3 antagonizes innate immune response to promote bovine alphaherpesvirus 1 replication via the DDIT3-SQSTM1-STING pathway.Virulence · 2022Article
- Review
- Genetic regulation of iron homeostasis in sideropenic patients with mild COVID-19 disease under a new oral iron formulation: Lessons from a different perspective.Immunobiology · 2022Article
- Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Induction of the unfolded protein response (UPR) is an adaptive cellular response to endoplasmic reticulum (ER) stress that allows a cell to reestablish ER homeostasis. However, under severe and persistent ER stress, prolonged UPR may activate unique pathways that lead to cell death. In this study, we investigated the activation of the protein kinase R-like ER kinase (PERK) pathway of UPR in cells infected with the coronavirus infectious bronchitis virus (IBV) and its relationship with IBV-induced apoptosis. The results showed moderate induction of PERK phosphorylation in IBV-infected cells. Meanwhile, activating transcription factor 4 (ATF4) was upregulated at the protein level in the infected cells, resulting in the induction in trans of the transcription factor ATF3 and the proapoptotic growth arrest and DNA damage-inducible protein GADD153. Knockdown of PERK by small interfering RNA (siRNA) suppressed the activation of GADD153 and the IBV-induced apoptosis. Interestingly, knockdown of protein kinase R (PKR) by siRNA and inhibition of the PKR kinase activity by 2-aminopurine (2-AP) also reduced the IBV-induced upregulation of GADD153 and apoptosis induction. In GADD153-knockdown cells, IBV-induced apoptosis was suppressed and virus replication inhibited, revealing a key role of GADD153 in IBV-induced cell death and virus replication. Analysis of the pathways downstream of GADD153 revealed much more activation of the extracellular signal-related kinase (ERK) pathway in GADD153-knockdown cells during IBV infection, indicating that GADD153 may modulate apoptosis through suppression of the pathway. This study provides solid evidence that induction of GADD153 by PERK and PKR plays an important regulatory role in the apoptotic process triggered by IBV infection.
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